Cardiovascular Disorders II Flashcards
Coronary Artery Disease (CAD)
aka Coronary Heart Disease (CHD) or Ischemic Heart Disease (IHD)
2nd leading cause of death in Canada
1 in 12 Canadian adults live with diagnosed heart disease
Left Main Coronary Artery (LMCA)
left side of heart muscle 2 branches a. left anterior descending (interventricular) - front and left side of heart b. circumflex - outer side and back of heart
Right Coronary Artery (RCA)
right side of heart muscle
right ventricle and atrium, SA and AV nodes
Pathophysiology of CAD
- decreased perfusion to myocardium due to occlusion of 1+ coronary arteries or branches
- inadequate blood supply to meet the myocardial oxygen demand
- myocardial ischemia
- myocardial death
Atherosclerosis
++ blood levels of lipids irritate or damage intima of arterial vessels
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fatty substances enter vessels after damaging the protective barrier, accumulate and form fatty streak
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smooth muscle cels move to intima to engulf fatty substance
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fibrous tissue formation and calcification
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atheroma grows, vessel wall becomes thick, fibrotic and calcified, lumen narrows
* impedes blood flow with risk for thrombosis
Collateral Circulation
with gradual occlusion of the larger vessels, the smaller collateral vessels increase in size and provide alternative channels for blood flow
CAD Risk Factors
Non-modifiable
a. age
b. sex (women, men have slightly higher risk at younger age)
c. family history (familial hypercholesterolemia, mutation on gene LDL receptors
Modifiable
a. serum lipid alterations (decreased HDL and increased LDL and triglycerides)
b. hypertension
c. smoking
d. diabetes mellitus (insulin resistance)
- endothelial damage
e. diet
f. obesity (lipid metabolism)
g. lack of physical activity
Cholesterol
serum lipid abnormality is responsible for atherogenesis
- it is what creates plaque
high triglyceride level with high HDL or low HDL increases risk for atherosclerosis
= lipid synthesized by the liver or ingested
= required for synthesis of certain hormones and bile salts
= insoluble in water, requires lipoprotein for transportation
Lipoproteins relevant to CAD
Very-low-density lipoproteins (VLDL)
- produced by liver and converted in blood stream to LDLs
- for delivery of TRIGLYCERIDES to non-hepatic tissue
Low-density lipoproteins (LDL)
- produced in liver as VLDL
- for delivery of mainly CHOLESTEROL to non-hepatic tissue
High-density lipoproteins (HDL)
- produced in liver and small intestine
- reverse cholesterol transport, helps to EXTRACT EXCESS CHOLESTEROL deposited in blood vessels back to liver for elimination
- antioxidant and anti-inflammatory functions
Metabolic Syndrome
specific risk factors markedly increase potential for heart disease
3 out of 5 conditions:
a. Waist circumference
Men > 102cm
Women > 88cm
b. Triglyceride levels
> 1.7 mmol/L
c. HDL cholesterol
Men < 1 mmol/L
Women < 1.3 mmol/L
d. BP
SBP > 130 mmHg
DBP > 85 mmHg
e. fasting glucose
> 5.6 mmol/L
Management of CAD
a. modify risk factors (control bp, diabetes, lifestyle, weight)
b. health promotion (identifying at risk, manage underlying condition)
c. nutrition therapy (complex carbohydrates, omega-3 fatty acids)
d. medications (cholesterol-lowering, anti-platelet agents)
Diagnostic tests of CAD
a. ECG detect myocardial ischemia b. Stress testing effects of exercise (stress) on heart c. Cardiac catheterization catheter through a peripheral artery into aorta and left heart under fluroscopic imaging d. Coronary angiography injection of contrast medium into coronary arteries to visualize lesions
Percutaneous Transluminal Coronary Angioplasty (PTCA)
blocked or narrowed portions of the artery are dilated with a catheter and inflated ballon to flatten plaque
may be followed by a mesh stent insertion to keep it open, may also prevent further plaque build up
Coronary Atherectomy
removal of plaques that form a blockage
- generally used BEFORE angioplasty balloon is inflated
- reduce blockage and force needed to inflate balloon
Coronary Bypass Grafting (CABG)
surgical intervention to bypass blockages between the aorta and the myocardium with grafting of vessels distal to the area of blockage
Myocardial Ischemia
occurs when blood flow to the heart muscle is obstructed by a partial or complete blockage of a coronary artery by a buildup of plaques
*myocardial O2 deficit greater than 20 mins = myocardial infarction
Stable angina (angina pectoris)
transient (<10 min) precordial discomfort or distressing sensation, typically provoked by exertion or stress, relieved by rest and the use of nitrates
result from: atherosclerosis
Unstable angina
anginal discomfort when resting or that awakens pt from sleep, caused by significant CAD
increased risk of progression to MI
result from: atherosclerosis with blood clot
Variant (prinzmetal) angina
chest discomfort with atypical characteristics, often occurs during rest, follows a cyclic or regular pattern of occurrence (same time each day)
result from: coronary artery spasm
Acute Coronary Syndromes (ACS)
sudden coronary obstruction caused by thrombus formation such that part of the heart muscle is unable to function properly
Three clinical manifestations:
a. unstable angina
b. ST Elevation Myocardial Infarction (STEMI)
c. Non-ST Elevation Myocardial Infarction (NSTEMI)
- less damage than STEMI
*sustained ischemia > myocardial infarction > myocardial inflammation and necrosis
Manifestations of Myocardial Ischemia
a. chest pain (may radiate to left arm, neck, jaw or shoulder blad)
- major subjective symptom, caused by decreased O2
b. shortness of breath
- left ventricular failure > pulmonary edema
c. diaphoresis, cool, clammy skin
- SNS stimulation
d. ++ HR and BP (initially)
- release of catecholamines
e. nausea and vomiting
- result of severe pain, vasovagal reflexes
f. fever (within first 24hr up to 1 week post)
- inflammatory process result from cell death
g. loss of consciousness
- inadequate cerebral perfusion
Myocardial Infarction (MI)
prolonged myocardial ischemia results in myocardial infarction MEDICAL EMERGENCY
occurs at the central zone of ischemic injury, zone of infarction
most MIs involve ventricles (especially left)
irreversible damage to the affected myocardium may result WITHIN 2-4 HRS without adequate perfusion, necrosis with subsequent scar formation or fibrosis
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permanent impairment of contraction ability
Classification of MI by extent
Transmural infarcts
= involve full thickness of ventricular wall, most commonly occur when there is obstruction of a single artery
Subendocardial infarcts
= involve the inner 1/3-1/2 of the ventricular wall, occurs more frequently in the presence of severely narrowed but still patent arteries
Intramural Infarcts
Subepicardial infarcts (outer wall)
Classification of MI by location
Anterior MI
= left anterior descending (LAD) artery occlusion, left ventricular failure (LVF)
Inferior MI
= right coronary artery (RCA) occlusion or circumflex occlusion
Septal MI
= left anterior descending (LAD) artery occlusion
Lateral MI
= circumflex occlusion
Diagnosis of MI
- a rise in plasma markers indicative of myocardial injury
- history of prolonged chest pain
- ECG abnormalities - characteristics of ischemia
Serum Cardiac Markers
released as a result of myocardial cell death
- Troponin I and Troponin T (cardiac specific)
- highly sensitive
- remains elevated for up to 10 days, not useful in reinfarction
Onset: 2-4 hr
Peak: 10-24hr
RTB: 10-14 days - CK-MB (creatine kinase with MB isoenzyme)
- high specificity for injury to myocardial tissue
- routine AMI marker
- false positive for significant skeletal injury and cardiac injury other than MI
Onset: 4-6 hr
Peak: 18-24 hr
RTB: 36-48 hr - Myoglobin
- low specificity, released in damage to other muscles
- most sensitive early marker
Onset: 1-3 hr
Peak: 6-12 hr
RTB: 24 hr
Heart’s Electrical System
- begins at SA node (right atrium) and spreads across right and left atria..atria contract
- signal arrives AV node (ventricles) allowing ventricles to fill
- signal moves through bundle of His (septum) and divided into left and right bundle branches through purkinje fibers (walls of ventricles)..ventricles contract
- L ventricle contracts an instant before R ventricle
ECG of normal sinus rhythm
P - atrial depolarization, SA node to atrial musculature
QRS - ventricular depolarization, activation of ventricles
T - repolarization, recovery
*ST end of ventricular depolarization to repolarization, significant for MI dx
ECG Changes
caused by necrotic, injured and ischemic zones of the infarcted area conduct impulses differently
a. prolonged Q wave
b. ST segment elevation
c. T wave inversion
Treatment of MI
a. rapid revascularization of occluded coronary artery
= restore blood flow: vasodilation, open artery (fibrinolysis - breakdown of fibrin in blood clot), PCI
= sublingual nitroglycerin: promote venous return, vasodilator, reduce workload
= beta-blockers: decrease oxygen demand, reduce HR, BP, contractility
b. adequate pain relief
= IV morphine (with vasodilator property)
c. manage life-threatening complications
= supplemental 02: maintain O2 content
= antiarrhythmics and beta-blockers: prevent dysrhythmia
= anti-platelet agents, anti-thrombotic agents
= reduce damage of necrosis
d. maximize physical and psychological well-being
= manage anxiety
e. rest
= reduce cardiac workload and O2 consumption
Changing practice of O2 therapy
use of oxygen only in hypoxemic patients
Thrombolytic Agents
= drugs used to dissolve blood and platelet clots
= best results occur if initiated 1-2 hours, magnitude of benefit declines after this period but some benefit achieved up to 12 hrs after onset
- must be low-risk candidate for complications caused by bleeding, may lead to hemorrhage
- reduce mortality and limit infarct size
Complications of MI: Ischemic
manifestation:
- reinfarction
- infarct extension
- angina
signaled by recurrent pain, ECG and enzyme changes
Complications of MI: Mechanical
manifestation:
- cardiac failure
damage to ventricle causing heart to no longer pump properly
treatment changes strength of contraction (inotropic agents such as dobutamine)
- cardiogenic shock
circulatory failure, inadequate perfusion to vital areas - mitral regurgitation
- ventricular aneurysm
- cardiac rupture
Complications of MI: Arrhythmic
manifestation:
- atrial or ventricular arrhythmia
common in the first 4 hrs
- sinus or atrioventricular node dysfunction
fibrillation, uncoordinated movement of cells, out of sync, fatal
Complications of MI: Embolic
manifestation: - CNS embolus stroke - peripheral embolus - left ventricular mural thrombus
thromboembolism, treated with thrombolytic or anticoagulant agents
Complications of MI: Inflammatory
manifestation:
- pericarditis
retrosternal discomfort/pain and fever associated with pericardial friction rub on auscultation
treated with aspirin or anti-inflammatory agents
Cardiac Rehabilitation
Rest, Exercise and Risk factor modification, Eat (RERE)
a. diet: low salt, low cholesterol, easy to digest to reduce workload
b. stool softener to prevent constipation and avoid straining
c. exercise program
d. smoking cessation, weight loss, stress reduction, control HTN and diabetes
